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      Ethyl pyruvate protects against sepsis by regulating energy metabolism

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          Abstract

          Background

          Ethyl pyruvate (EP) is a derivative of pyruvic acid that has been demonstrated to be a potential scavenger of reactive oxygen species as well as an anti-inflammatory agent. In this study, we investigated the protective effects of EP and its role in regulating the energy metabolism in the livers of cecal-ligation-and-puncture-induced septic mice.

          Methods

          The animals were treated intraperitoneally with 0.2 mL of Ringer’s lactate solution or an equivalent volume of Ringer’s lactate solution containing EP immediately after cecal ligation and puncture. Each mouse in the Sham group was only subjected to a laparotomy. At 30-, 60-, 180-, and 360-minute time points, we measured the histopathological alterations of the intestines, and the plasma levels of interleukin (IL)-1β, IL-6, IL-10, and tumor necrosis factor-α, and the total antioxidative capacity, malondialdehyde content, and lactate and lactate/pyruvate levels in livers. Furthermore, we detected the levels of adenosine triphosphate, total adenylate, and energy charge in the livers.

          Results

          Our results demonstrated that the administration of EP significantly improved the survival rate and reduced intestinal histological alterations. EP inhibited the plasma levels of IL-1β, IL-6, and tumor necrosis factor-α and increased the IL-10 level. EP significantly inhibited the elevation of the malondialdehyde, lactate, and lactate/pyruvate levels and enhanced the total antioxidative capacity levels in the liver tissues. The downregulation of the adenosine triphosphate, total adenylate, and energy charge levels in the liver tissues was reversed in the septic mice treated with EP.

          Conclusion

          The results suggest that EP administration effectively modulates the energy metabolism, which may be an important component in treatment of sepsis.

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          Most cited references 25

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          Intestinal mucosal lesion in low-flow states. I. A morphological, hemodynamic, and metabolic reappraisal.

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            Mitochondrial dysfunction in septic shock and multiple organ dysfunction syndrome.

            Sepsis is the leading cause of death in medical intensive care units. In most fatal cases of sepsis the patient experiences an insidious, progressive decline in vital organ function, i.e. multiple organ dysfunction syndrome (MODS), which is commonly associated with signs of accelerated anaerobic metabolism despite supernormal systemic oxygen delivery. Based on this clinical scenario, tissue hypoxia has long been considered the putative mechanism of MODS. However, efforts to enhance tissue oxygenation during severe sepsis have proved ineffective, and a growing body of evidence indicates that mitochondria contribute significantly to the pathogenesis of sepsis-induced MODS. In addition to dysregulation of oxygen metabolism ('cytopathic hypoxia'), sepsis-induced mitochondrial dysfunction contributes to organ injury through accelerated oxidant production and by promoting cell death. Advances in our understanding of the mechanisms of mitochondrial damage and in its detection could revolutionize the management of this devastating disease.
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              The association of sepsis syndrome and organ dysfunction with mortality in emergency department patients with suspected infection.

              The critical care community has used standard criteria for defining the sepsis syndromes and organ dysfunction for more than 15 years; however, these criteria are not well validated in the emergency department (ED) setting. The study objectives in our ED population of patients admitted to the hospital are to determine the prevalence of the sepsis syndromes, quantify inhospital mortality and 1-year survival associated with the sepsis syndromes, and assess the inhospital and 1-year survival associated with organ dysfunctions. This was a prospective, observational, cohort study from February 1, 2000, to February 1, 2001 in an urban university hospital ED with 50,000 annual visits. There were 3,102 (96% of eligible) consecutive adult patients (aged 18 years or older) with suspected infection (as indicated by the clinical decision to obtain a blood culture) who were enrolled. Patients were screened for systemic inflammatory response syndrome (SIRS) (2 or more indicators of inflammatory response), sepsis (SIRS plus suspected infection), severe sepsis (sepsis plus organ dysfunction), septic shock (sepsis plus hypotension refractory to an initial fluid challenge), and number of organs with acute dysfunction. Main outcome measure was inhospital and 1-year mortality. Overall inhospital mortality was 4.1% and 1-year mortality was 22%. The inhospital mortality rates were suspected infection without SIRS 2.1%, sepsis 1.3%, severe sepsis 9.2%, and septic shock 28%. Compared to suspected infection without SIRS, adjusted risks of inhospital mortality were severe sepsis (odds ratio [OR] 4.0; 95% confidence interval [CI] 2.6 to 6.3) and septic shock (OR 13.8; 95% CI 6.6 to 29). Severe sepsis (OR 2.2; 95% CI 1.8 to 2.6) and septic shock (OR 3.5; 95% CI 2.3 to 5.3) also predicted 1-year mortality. The presence of SIRS criteria alone had no prognostic value for either endpoint. Each additional organ dysfunction increased the adjusted 1-year mortality hazard by 82% (pulse rate: 1.82, 95% CI 1.7 to 2.0). Immediate identification of acute organ dysfunction in ED patients with suspected infection may help select patients at increased short- and long-term mortality risk. SIRS criteria offered no additional prognostic value, whereas each additional organ dysfunction increased the 1-year mortality risk.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2016
                23 February 2016
                : 12
                : 287-294
                Affiliations
                [1 ]Department of Critical Care Medicine, Chinese PLA General Hospital, Beijing, People’s Republic of China
                [2 ]Department of Critical Care Medicine, The Centre Hospital of BaoTou, BaoTou, People’s Republic of China
                Author notes
                Correspondence: Feihu Zhou, Department of Critical Care Medicine, Chinese PLA General Hospital, 28 Fuxing Road, Haidian District, Beijing 100853, People’s Republic of China, Tel +86 138 1091 8398, Fax +86 10 6816 8834, Email feihuzhou301@ 123456126.com
                Article
                tcrm-12-287
                10.2147/TCRM.S97989
                4770074
                26966369
                © 2016 Kang et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Medicine

                reactive oxygen species, inflammation, energy metabolism, ethyl pyruvate, sepsis

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